Evidence map›Paper›PMID 12610208›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Molecular classification of familial non-BRCA1/BRCA2 breast cancer.

Ingrid Hedenfalk, Markus Ringner, Amir Ben-Dor, Zohar Yakhini, Yidong Chen, Gunilla Chebil, Robert Ach, Niklas Loman, Håkan Olsson, Paul Meltzer and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed.

  1. Article
  2. GermlineFrontiers in genetics · 2020
    Article
  3. Reparameterization of PAM50 Expression Identifies Novel Breast Tumor Dimensions and Leads to Discovery of a Genome-Wide Significant Breast Cancer Locus atCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Pathology of hereditary breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2011
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Ingrid HedenfalkCancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Markus Ringner
Amir Ben-Dor
Zohar Yakhini
Yidong Chen
Gunilla Chebil
Robert Ach
Niklas Loman
Håkan Olsson
Paul Meltzer
Ake Borg
Jeffrey Trent

Funding

MOLECULAR CYTOGENETICS OF GENE AMPLIFICATIONZ01HG000037 · NHGRI · HUMAN GENOME RESEARCH · PI MELTZER, PAUL S. · 1995 to 2004
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Functional genomics of cancerZ01HG000186 · NHGRI · HUMAN GENOME RESEARCH · PI MELTZER, PAUL S. · 2001 to 2005
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6 · The paper itself

Abstract

In the decade since their discovery, the two major breast cancer susceptibility genes BRCA1 and BRCA2, have been shown conclusively to be involved in a significant fraction of families segregating breast and ovarian cancer. However, it has become equally clear that a large proportion of families segregating breast cancer alone are not caused by mutations in BRCA1 or BRCA2. Unfortunately, despite intensive effort, the identification of additional breast cancer predisposition genes has so far been unsuccessful, presumably because of genetic heterogeneity, low penetrance, or recessive/polygenic mechanisms. These non-BRCA1/2 breast cancer families (termed BRCAx families) comprise a histopathologically heterogeneous group, further supporting their origin from multiple genetic events. Accordingly, the identification of a method to successfully subdivide BRCAx families into recognizable groups could be of considerable value to further genetic analysis. We have previously shown that global gene expression analysis can identify unique and distinct expression profiles in breast tumors from BRCA1 and BRCA2 mutation carriers. Here we show that gene expression profiling can discover novel classes among BRCAx tumors, and differentiate them from BRCA1 and BRCA2 tumors. Moreover, microarray-based comparative genomic hybridization (CGH) to cDNA arrays revealed specific somatic genetic alterations within the BRCAx subgroups. These findings illustrate that, when gene expression-based classifications are used, BRCAx families can be grouped into homogeneous subsets, thereby potentially increasing the power of conventional genetic analysis.

Indexed as

Genes, BRCA1MutationAdultAgedBRCA2 ProteinBreast NeoplasmsChromosome MappingDNA, ComplementaryDown-RegulationFemaleHumansMiddle AgedNucleic Acid HybridizationOligonucleotide Array Sequence AnalysisUp-RegulationBRCA2 ProteinDNA, Complementary

Identifiers

PMID12610208
PMCPMC151375

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.